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201316Mar13:52

Hope for threat­ened Tas­man­ian devils

Infor­ma­tion
pub­lished 16 March 2013 | mod­i­fied 19 Octo­ber 2016
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Tasmanian devil healthyRecently some opti­mism came over peo­ple involved with Tas­man­ian devil con­ser­va­tion. Although the devil num­bers are still plum­met­ing because of the Devil Facial Tumour Dis­ease (DFTD) and extinc­tion is on the lure, there is still a hope amongst devil researchers. Since the dis­ease was dis­cov­ered in 1996, in some areas more than 90% of the Tas­man­ian devil pop­u­la­tion has been wiped out. The facial can­cer, which spreads when the dev­ils bite each other’s faces dur­ing fight­ing, kills its vic­tims in a mat­ter of months.

We can be con­fi­dent that we’re not going to see extinc­tion of the Tas­man­ian devil because we’ve got this insur­ance pop­u­la­tion — it’s well main­tained, it’s genet­i­cally rep­re­sen­ta­tive of the wild population
« Dr Phil Bell, man­ager of the Save the Tas­man­ian Devil Pro­gram

Nev­er­the­less, con­ser­va­tion efforts now have achieved a sig­nif­i­cant vic­tory with the estab­lish­ment of a large, genet­i­cally diverse insur­ance pop­u­la­tion of cap­tive dev­ils in zoos and wildlife insti­tu­tions around Aus­tralia.

In addi­tion sci­en­tists are des­per­ate to find out more about the mys­te­ri­ous can­cer which some­how man­ages to evade the dev­ils’ immune sys­tem. Their research could pave the way for the devel­op­ment of a vac­cine for this con­ta­gious can­cer.

Tasmanian devil dftdUntil now, sci­en­tists have believed that the tumours were able to avoid detec­tion by the immune sys­tem because the Tas­man­ian dev­ils have very lit­tle genetic diver­sity (pre­vent­ing the immune sys­tem from recog­nis­ing the tumour as for­eign). How­ever, a Uni­ver­sity of Cam­bridge led col­lab­o­ra­tion with the Uni­ver­si­ties of Tas­ma­nia, Syd­ney and South Den­mark has dis­cov­ered that the expla­na­tion is more com­plex.

On the sur­face of nearly every mam­malian cell are major his­to­com­pat­i­bil­ity com­plex (MHC) mol­e­cules. These mol­e­cules enable the immune sys­tem to deter­mine if a cell is friend or foe, trig­ger­ing an immune response if the cell is for­eign and a poten­tial threat. The new research, pub­lished on 11 March, in the jour­nal PNAS, reveals that DFTD can­cer cells lack these crit­i­cal mol­e­cules, thereby avoid­ing detec­tion by the dev­ils’ immune system.

Devel­op­ing a vac­cine based on our research could tip the bal­ance in the favour of the devil and give them a fight­ing chance
Dr Han­nah Sid­dle, lead author, Uni­ver­sity of Cam­bridge »


Pro­fes­sor Jim Kauf­man, from the Uni­ver­sity of Cambridge’s Depart­ment of Pathol­ogy, said: “Once it was found that the can­cer was escap­ing from the dev­ils’ immune sys­tem, sci­en­tists needed to fig­ure out how.”

The researchers found that the DFTD cells have lost the expres­sion of MHC mol­e­cules, but that the genes that code for these mol­e­cules are still intact. This means that these genes could poten­tially be turned back on. Indeed, the sci­en­tists showed that by intro­duc­ing sig­nalling mol­e­cules such as interferon-​gamma, a pro­tein which trig­gers the immune response, the DFTD cells can be forced to express MHC mol­e­cules.

Dr Han­nah Sid­dle, lead author of the paper from the Uni­ver­sity of Cam­bridge, said: “Devel­op­ing a vac­cine based on our research could tip the bal­ance in the favour of the devil and give them a fight­ing chance. How­ever, we still face some hur­dles. The tumour is evolv­ing over time and any vac­cine pro­gramme would have to take this into con­sid­er­a­tion. Also, because of the dif­fi­cul­ties of vac­ci­nat­ing a wild pop­u­la­tion, it may be more effi­cient to use a vac­cine in the con­text of return­ing cap­tive dev­ils to the wild.”

Although the only other con­ta­gious can­cer has been found in dogs (canine trans­mis­si­ble vene­real can­cer), the rapid devel­op­ment of DFTD high­lights how quickly they can emerge.

Pro­fes­sor Kauf­man added: “Our study has impli­ca­tions beyond the Tas­man­ian devil. Sooner or later a human strain of con­ta­gious can­cer will develop, and this work gives us insight into how these dis­eases emerge and evolve.”


The above news item is reprinted from mate­ri­als avail­able at ECOS mag­a­zine and Uni­ver­sity of Cam­bridge. Orig­i­nal text may be edited for con­tent and length.
(Source: ECOS mag­a­zine, 25.02.2013; Uni­ver­sity of Cam­bridge News, 11.03.2013)

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